IL-1a can readily release pro-inflammatory alarmins during cell necrosis, causing local tissue inflammation, and IL-1b promotes systemic inflammation primarily by initiating acute phase response proteins (such as C-reactive protein) in the liver, activating endothelial cells, triggering fever, mobilizing neutrophils (leukocytosis), and activating all types of leukocytes.[50] A clinical study shows that IL-1b inhibitors reduce the incidence of major adverse cardiovascular events in patients with high-risk atherosclerosis in CKD.[51]. The gene discussed is IL1A; the disease is atherosclerosis.